Molecular layer ectopias and microgyria have been seen in the brains of dyslexic subjects. Immune-defective mice spontaneously develop molecular layer ectopias, and we have successfully induced microgyria in rats and mice. These minor cortical abnormalities have their origin during the end of neuronal migration to the neocortex, but little is known about the exact mechanisms that produce them. Epidemiologic considerations could implicate immune pathology both in dyslexics and in the mice. Both in the spontaneous form (SMM) and in the induced form (IMM), we suspect that exact timing and severity of the pathogenic insult determines the ultimate morphology and behavioral consequences of the lesion. In the proposed research, we will elucidate the earliest date or origin of SMM in immune- defective mice and its cellular nature at the onset. We will describe the injurious nature of the onset of SMM and IMM and the role of immunopathology in the onset of SMM in the immune-defective mice. We will specify the effect of timing and severity of the insult on the type of IMM that results, the developmental time course of SMM and IMM from onset to maturity. Minor cortical malformations in humans are receiving increasing attention, but their etiology and significance are unknown. We have seen them to be related to at least one form of learning disability -- developmental dyslexia. We expect that this research will shed light on the origin of minor cortical malformations.